Hornnes P, Kühl C, Klebe J G
Diabetologia. 1978 Sep;15(3):165-8. doi: 10.1007/BF00421233.
In order to investigate whether an increased gastrointestinal potentiation of glucose-induced insulin release might be involved in the enhanced insulin response to oral glucose in pregnancy, seven normal women were subjected to an oral glucose tolerance test (OGTT) and an IV glucose infusion test (IVGI) in the last trimester of pregnancy and again four to ten weeks post-partum. The amount of glucose administered intravenously was adjusted to obtain plasma glucose concentrations similar to those of the preceding OGTT. By this technique it was possible to quantitate the amount of insulin release attributable to gastrointestinal factors. Contrary to expectations, the results revealed that the gastrointestinal potentiation of insulin secretion was reduced by more than 75% in late pregnancy (p less than 0.05). The hyperinsulinaemia of pregnancy is therefore not explained by an increased activity of the entero-insular axis. Moreover the results confirm a substantially increased beta cell sensitivity to a glycaemic stimulus in pregnancy.
为了研究胃肠道对葡萄糖诱导的胰岛素释放增强作用增加是否可能与孕期口服葡萄糖后胰岛素反应增强有关，对7名正常女性在妊娠晚期进行了口服葡萄糖耐量试验（OGTT）和静脉葡萄糖输注试验（IVGI），产后4至10周再次进行上述试验。静脉注射的葡萄糖量经过调整，以使血浆葡萄糖浓度与之前OGTT时相似。通过这种技术，可以定量归因于胃肠道因素的胰岛素释放量。与预期相反，结果显示妊娠晚期胰岛素分泌的胃肠道增强作用降低了75%以上（p<0.05）。因此，孕期高胰岛素血症不能用肠-胰岛轴活性增加来解释。此外，结果证实孕期β细胞对血糖刺激的敏感性大幅增加。
